Potentiation of (-)-epigallocatechin-3-gaUate-induced apoptosis by bortezomib. in multiple myeloma cells.pdf
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ActaBiochimBiophysSinf2009):1018—1026I@TheAuthor2009.PublishedbyABBSEditorialOfficeinassociationwithOxfordUniversityPressonbehalfof
theInstituteofBiochemistryandCellBiology,ShanghaiInstitutesforBiologicalSciences,ChineseAcademyofSciences.DOI:10.10g3/abbsg『mp0g4. ABBS
AdvanceAccessPublication10November2009
Potentiationof(一)-epigaUocatechin一3-gallate—inducedapoptosisbybortezomib
inmultiplemyelomacells
QingWang,JuanLi,JingliGu,BeihuiHuang,YingZhao,DongZheng,YanDing,andLijinZeng
DepartmentofHematology,TheFirstAffiliatedHospital,SunYat—senUniversity,Guangzhou510080,China
Correspondenceaddress.Tel:+86—208831:Fax:+86—20E—mail:luliyuan@tom.corn
The green tea constituent, (一)一epigallocatechin一3一 numberofcellularprocessesand itse衔cacy in many
gallate (EGCG),haschemopreventiveandanticancer tun3ormodelsystems 3『,41.Themechanism underlying
effects.Thisispartiallybecauseoftheselectiveabliity EGCG—mediatedapoptosisofcancercellsisincomple—
ofEGCG to induceapoptosisanddeath incancercells telyunderstood.Suchanunderstanding,however,could
withoutaffectingnormalcells.Inthepresentstudy,the provetheimportanceofdevelopingEGCG andrelated
activityofEGCG againstthemyelomacellline.KM3. compoundsas single agentsor in combination with
wasexamined.Ourresultsdemonstrated.forthefirst otherdrugsforthepreventionand/ortherapyofcancer.
time.that the treatmentofthe KM 3 cellline with Thetranscriptionfactor.NF.KB.playsacriticalrolein
EGCG inhibitscellproliferationand inducesapoptosis. theregulation ofgenesrelatedtoeel1surviva1.prolifer.
andthereisasynergisticeffectwhenEGCG andborte. ation,andapoptosis[5,6].Undernormalconditions,
zomibarecombined.Furtherexperimentsshowed~that NF—KB ispresentinthecytoplasm asaninactivehetero.
thiseffectinvolvestheNF.KB pathway.EGCG inhibits trimerconsistingofP50,P65,andIK
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